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G-0967 Coronary Arte..
G-0967 Coronary Arte..
G-0967 Coronary Arte..
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G-0967 Coronary Arte..

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  • 1. Coronary Artery Disease, Angina, Myocardial Infarction, and Congestive Heart Failure Provided Courtesy of RD411.com Where dietitians go for information Review Date 3/09 G-0967 A Review of the Basics
  • 2. <ul><li>Smoking </li></ul><ul><li>High intake of alcohol </li></ul><ul><li>Obesity </li></ul><ul><li>Sedentary lifestyle </li></ul><ul><li>Diabetes </li></ul><ul><li>Hypercholestrolemia </li></ul><ul><li>Hyperlipidemia </li></ul>Risk Factors For Coronary Artery Disease, Angina, Myocardial Infarction, and Congestive Heart Failure
  • 3. <ul><li>More than 45 years old for males and 55 years old for females (risk increases after menopause) </li></ul><ul><li>Family history—genetics </li></ul><ul><li>Hypertension </li></ul><ul><li>Stress/personality type </li></ul>Risk Factors (cont’d) For Coronary Artery Disease, Angina, Myocardial Infarction, and Congestive Heart Failure
  • 4. <ul><li>High low-density lipoprotein (LDL) cholesterol </li></ul><ul><li>Low high-density lipoprotein (HDL) cholesterol </li></ul><ul><li>Left ventricular hypertrophy </li></ul>Risk Factors (cont’d) For Coronary Artery Disease, Angina, Myocardial Infarction, and Congestive Heart Failure
  • 5. <ul><li>Anyone with cardiac conditions </li></ul><ul><ul><li>Coronary artery disease (CAD) </li></ul></ul><ul><ul><li>Myocardial infarction (MI) </li></ul></ul><ul><ul><li>Postcoronary bypass </li></ul></ul><ul><li>Hypertension </li></ul><ul><li>Left ventricular hypertrophy </li></ul><ul><li>Diabetes </li></ul><ul><li>Chronic obstructive pulmonary disease </li></ul>Risk Factors For Congestive Heart Failure
  • 6. <ul><li>Pulmonary hypertension </li></ul><ul><li>Anemia </li></ul><ul><li>Hypothyroidism </li></ul><ul><li>Hyperthyroidism </li></ul><ul><li>Overweight or obesity </li></ul><ul><li>Alcoholism </li></ul>Risk Factors (cont’d) For Congestive Heart Failure
  • 7. <ul><li>Blood flow to the vessels surrounding the heart is blocked </li></ul><ul><li>The major underlying cause of CAD is atherosclerosis </li></ul>Coronary Artery Disease: An Overview
  • 8. <ul><li>Elevated cholesterol and triglyceride levels </li></ul><ul><li>Hypertension </li></ul><ul><li>Infection that initiates the inflammatory response </li></ul>Plaque Development Many factors speed up plaque development:
  • 9. <ul><li>Elevated iron levels—carry free radicals that damage lining </li></ul><ul><li>Elevated homocysteine level </li></ul><ul><li>Cigarette smoking </li></ul><ul><li>Diabetes </li></ul><ul><li>Obesity </li></ul><ul><li>Oxidized LDL cholesterol </li></ul>Plaque Development (cont’d) Many factors speed up plaque development:
  • 10. <ul><li>Buildup of smooth muscle cells, macrophages, and lymphocytes </li></ul><ul><li>Smooth muscle cells form a matrix of connective tissue </li></ul><ul><li>Lipid and cholesterol accumulates in the matrix </li></ul>The Atherosclerotic Process
  • 11. <ul><li>Lipid deposits and other materials (including cellular waste, fibrin, and calcium) build up and form a plaque </li></ul><ul><li>After injury, platelets adhere to the arterial wall and release growth factors, which promote lesion development </li></ul>The Atherosclerotic Process (cont’d)
  • 12. <ul><li>Fatty streaks form, often in people younger than 30 years of age </li></ul><ul><li>People are asymptomatic during this first stage of CAD </li></ul><ul><li>Plasma LDL enters the injured endothelial wall and forms a plaque that sometimes is prone to rupture </li></ul>Development of Coronary Artery Disease Steps to development of CAD:
  • 13. <ul><li>Acute, complicated lesions with rupture and either nonocclusive or occlusive thrombus form </li></ul><ul><ul><li>Occlusive often results in MI and sudden death </li></ul></ul><ul><li>Hemorrhage into plaque produces thrombi; thrombus formation within arterial lumen initiated </li></ul>Development of Coronary Artery Disease (cont’d) Steps to development of CAD:
  • 14. <ul><li>Progressive narrowing of lumen </li></ul><ul><li>Insufficient blood flow to myocardium (ischemia) results </li></ul><ul><li>Chest pain or angina pectoris occurs </li></ul>Development of Coronary Artery Disease (cont’d) Steps to development of CAD:
  • 15. <ul><li>Chest pain </li></ul><ul><li>Hypertension </li></ul><ul><li>Increased pulse </li></ul><ul><li>Increased respiration </li></ul><ul><li>Dyspnea on exertion </li></ul><ul><li>Pallor of skin </li></ul><ul><li>Lightheadedness with exertion </li></ul>Signs and Symptoms of Coronary Artery Disease
  • 16. <ul><li>Diminished peripheral pulses </li></ul><ul><li>Intermittent claudication—cramping of the lower extremities </li></ul>Signs and Symptoms of Coronary Artery Disease (cont’d)
  • 17. <ul><li>Antihyperlipidemic agents </li></ul><ul><li>Medications that lower triglycerides </li></ul><ul><li>Antiplatelets (aspirin) </li></ul><ul><li>Antihypertensives </li></ul><ul><li>Antianginals (nitroglycerin) </li></ul><ul><li>Antimicrobials </li></ul>Treatment of Coronary Artery Disease
  • 18. <ul><li>Chest pain caused by myocardial ischemia from reduced blood flow and/or reduced oxygen supply to myocardium </li></ul><ul><li>Angina is a warning sign that a heart attack (MI) may occur </li></ul>Angina Pectoris: An Overview
  • 19. <ul><li>Aerobic metabolism switches to anaerobic metabolism: </li></ul><ul><ul><li>Lactic acid buildup </li></ul></ul><ul><ul><li>Release of histamine, bradykinins, and enzymes, which stimulate nerve fibers in myocardium, sending pain impulses to the central nervous system </li></ul></ul>Angina Pectoris: An Overview (cont’d)
  • 20. <ul><li>Other causes of decreased oxygen supply to myocardium: </li></ul><ul><ul><li>Congestive heart failure </li></ul></ul><ul><ul><li>Congenital heart defects </li></ul></ul><ul><ul><li>Pulmonary hypertension </li></ul></ul><ul><ul><li>Left ventricular hypertrophy </li></ul></ul><ul><ul><li>Cardiomyopathy </li></ul></ul><ul><ul><li>Severe hypertension </li></ul></ul><ul><ul><li>Narrowing of aortic valve </li></ul></ul>Angina Pectoris: An Overview (cont’d)
  • 21. <ul><li>Other causes of decreased oxygen supply to myocardium (cont’d) : </li></ul><ul><ul><li>Leakage of the aortic valve </li></ul></ul><ul><ul><li>Ventricle wall thickening </li></ul></ul><ul><ul><li>Atheroma leading to arterial narrowing </li></ul></ul><ul><li>Silent ischemia—decreased oxygen supply with no pain </li></ul>Angina Pectoris: An Overview (cont’d)
  • 22. <ul><li>Anemia </li></ul><ul><li>Exercise </li></ul><ul><li>Thyrotoxicosis </li></ul><ul><li>Substance abuse, particularly cocaine </li></ul><ul><li>Hyperthyroidism </li></ul><ul><li>Emotional stress </li></ul>Causes of Increased Oxygen Demand of Myocardium
  • 23. <ul><li>Stable: </li></ul><ul><ul><li>Caused by specific amount of activity </li></ul></ul><ul><ul><li>Predictable </li></ul></ul><ul><ul><li>Relieved with rest and nitrates </li></ul></ul><ul><li>Unstable: </li></ul><ul><ul><li>Pain occurs with increasing frequency, severity, and duration over time </li></ul></ul><ul><ul><li>Unpredictable </li></ul></ul><ul><ul><li>May occur at rest </li></ul></ul><ul><ul><li>High risk for MI </li></ul></ul>Four Types of Angina
  • 24. <ul><li>Prinzmetal’s (variant): </li></ul><ul><ul><li>No identified cause </li></ul></ul><ul><ul><li>May occur at same time of day </li></ul></ul><ul><ul><li>May intensify or worsen over time </li></ul></ul><ul><ul><li>Usual cause is coronary artery spasm </li></ul></ul><ul><li>Angina decubitus: </li></ul><ul><ul><li>Occurs when a person is lying down with no cause </li></ul></ul><ul><ul><li>Occurs because gravity redistributes body fluids </li></ul></ul>Four Types of Angina (cont’d)
  • 25. <ul><li>Form of angina caused by neither spasm or blockage of the large coronary arteries </li></ul><ul><li>Temporary narrowing of the small coronary arteries possibly responsible </li></ul><ul><li>Reasons for temporary narrowing are unknown, but possibly because of chemical imbalance in the heart or abnormal functioning of the small arteries </li></ul>Syndrome X
  • 26. <ul><li>Pressure or heaviness in chest beneath breastbone—women are likely to have unusual types of chest discomfort </li></ul><ul><li>Pain may occur down shoulder or inside of arms, or in the throat, jaw, or teeth </li></ul><ul><li>Stomach pain, especially after eating </li></ul><ul><li>Sweating </li></ul>Signs and Symptoms of Angina
  • 27. <ul><li>Light-headedness </li></ul><ul><li>Hypotension </li></ul><ul><li>Pulse changes </li></ul><ul><li>Indigestion </li></ul>Signs and Symptoms of Angina (cont’d)
  • 28. <ul><li>Antianginals (nitroglycerin) </li></ul><ul><li>Antiplatelets (aspirin) </li></ul><ul><li>ACE inhibitors </li></ul><ul><li>Beta-blockers </li></ul><ul><li>Calcium channel-blockers </li></ul><ul><li>Thrombolytic therapy (if thrombi are cause) </li></ul>Treatment of Angina
  • 29. <ul><li>Stool softeners </li></ul><ul><li>Oxygen administration </li></ul><ul><li>Percutaneous transluminal coronary angioplasty (PTCA) or coronary artery bypass graft (CABG) to prevent MI </li></ul>Treatment of Angina (cont’d)
  • 30. <ul><li>Death of cells in the myocardium, usually related to prolonged or severe ischemia </li></ul><ul><li>Necrosis, tissue damage, and sometimes death result </li></ul>Myocardial Infarction: An Overview
  • 31. <ul><li>Cause of MI include: </li></ul><ul><ul><li>Sudden onset of ventricular fibrillation </li></ul></ul><ul><ul><li>Embolus (most common cause) </li></ul></ul><ul><ul><li>Thrombosis </li></ul></ul><ul><ul><li>Artherosclerotic occlusion </li></ul></ul><ul><ul><li>Prolonged vasospasm </li></ul></ul>Myocardial Infarction: An Overview (cont’d)
  • 32. <ul><li>Cellular injury occurs from lack of oxygen; if prolonged, will lead to cell death </li></ul><ul><li>Scar replaces muscle, but can not contract or conduct impulses; location of damage is determined by which artery is blocked </li></ul><ul><li>Damage begins at subendocardial level; will progress to the epicadium with 1-6 hours </li></ul>Progression of Myocardial Infarction
  • 33. <ul><li>Damaged cells lead to decreased contractility </li></ul><ul><ul><li>Less blood ejected by left ventricle with each beat </li></ul></ul><ul><ul><li>Decreased blood pressure </li></ul></ul><ul><ul><li>Decreased tissue perfusion </li></ul></ul>Progression of Myocardial Infarction (cont’d)
  • 34. <ul><li>Pain—typical is middle of chest, radiating to jaws, arms (usually the left), abdomen, and/or shoulders, and lasting about 20 minutes </li></ul><ul><ul><li>Possible to have no pain or atypical pain (particularly in females) </li></ul></ul><ul><ul><li>Sudden onset of pain, not associated with activity </li></ul></ul>Signs and Symptoms of Myocardial Infarction
  • 35. <ul><li>Tachycardia </li></ul><ul><li>Excessive perspiration </li></ul><ul><li>Painful breathing and/or difficulty breathing </li></ul><ul><li>Anxiety/panic </li></ul><ul><li>Nausea/vomiting </li></ul><ul><li>Fever </li></ul><ul><li>Stomach pain, often confused with indigestion </li></ul>Signs and Symptoms of Myocardial Infarction (cont’d)
  • 36. <ul><li>Creatinine phosphokinase (CPK): </li></ul><ul><ul><li>Not elevated in blood serum, unless injury has occurred </li></ul></ul><ul><ul><li>CPK II is present in heart tissue and is elevated if MI has occurred </li></ul></ul>Cardiac Enzymes
  • 37. <ul><li>Lactic dehydrogenase (LDH): </li></ul><ul><ul><li>LDH I is present in cardiac muscle, and LDH II is present in the reticuloendothelial system </li></ul></ul><ul><ul><li>Usually LDH I is greater than LDH II, but following a MI, LDH II is greater than LDH I </li></ul></ul><ul><li>Troponin: </li></ul><ul><ul><li>Involved in muscle contraction and released when cells are damaged </li></ul></ul>Cardiac Enzymes (cont’d)
  • 38. <ul><li>If more than 50% of heart tissue is damaged, severe disability or death will result </li></ul><ul><li>Pericarditis may develop up to 2 months later: </li></ul><ul><ul><li>Fever </li></ul></ul><ul><ul><li>Pericardial effusion </li></ul></ul><ul><ul><li>Pleurisy </li></ul></ul><ul><ul><li>Pleural effusion </li></ul></ul><ul><ul><li>Joint pain </li></ul></ul>Complications of Myocardial Infarction
  • 39. <ul><li>Rupture of heart muscle </li></ul><ul><li>Ventricular aneurysm </li></ul><ul><li>Blood clots </li></ul><ul><li>Hypotension </li></ul>Complications of Myocardial Infarction (cont’d)
  • 40. <ul><li>Antianginals (nitroglycerin) </li></ul><ul><li>Analgesics </li></ul><ul><li>Stool softener </li></ul><ul><li>Electrolyte replacement </li></ul><ul><li>Calcium channel-blockers </li></ul><ul><li>Beta-blockers </li></ul><ul><li>Antihypertensives </li></ul><ul><li>Anticoagulants </li></ul>Treatment Following Myocardial Infarction
  • 41. <ul><li>Antiarrhythmics </li></ul><ul><li>Thrombolytics </li></ul><ul><li>Oxygen </li></ul><ul><li>Mild antianxiety agents </li></ul>Treatment Following Myocardial Infarction (cont’d)
  • 42. <ul><li>Inability of the heart to pump sufficiently to meet metabolic needs, leading to decreased tissue perfusion as a result of decreased cardiac output </li></ul><ul><li>Acute or chronic </li></ul>Congestive Heart Failure: An Overview
  • 43. <ul><li>MI </li></ul><ul><li>Hypertension </li></ul><ul><li>Myocarditis </li></ul><ul><li>Pulmonary embolism </li></ul><ul><li>CAD </li></ul><ul><li>Kidney failure </li></ul><ul><li>Cardiomyopathies </li></ul>Causes of Congestive Heart Failure
  • 44. <ul><li>Valve disorders </li></ul><ul><li>Inflammatory conditions </li></ul><ul><li>Water intoxication </li></ul><ul><li>Side effects of medicine, such as corticosteroids </li></ul>Causes of Congestive Heart Failure (cont’d)
  • 45. <ul><li>Damage to the heart leads to decreased output and tissue perfusion </li></ul><ul><li>Andrenergic nervous system, renin-angiotensin system, and cytokine system are activated to compensate for the damage </li></ul>Development of Congestive Heart Failure
  • 46. <ul><li>Decreased cardiac output causes release of norepinepherine to increase heart rate and contractility </li></ul><ul><ul><li>Causes vasoconstriction </li></ul></ul><ul><ul><li>Increases cardiac output </li></ul></ul>Development of Congestive Heart Failure (cont’d)
  • 47. <ul><li>Decreased cardiac output decreases renal perfusion and activation of the renin-angiotensin-aldosterone system </li></ul><ul><ul><li>Causes vasoconstriction and leads to the production of aldosterone and antidiuretic hormone (ADH) </li></ul></ul><ul><ul><li>Aldosterone causes sodium reabsorption and water retention—blood pressure increases </li></ul></ul><ul><ul><li>ADH inhibits water excretion and raises blood pressure </li></ul></ul>Development of Congestive Heart Failure (cont’d)
  • 48. <ul><li>Vasoconstriction causes increased blood return to heart:* </li></ul><ul><ul><li>Causing more stretch of the heart muscle and enlargement of the heart chambers </li></ul></ul><ul><ul><li>Increasing cardiac output in the short term </li></ul></ul>Development of Congestive Heart Failure (cont’d) *Frank-Starling law: The greater the stretch of cardiac muscle fibers, the greater the force of contraction.
  • 49. <ul><li>Ventricular hypertrophy results from excess fluid and pressure: </li></ul><ul><ul><li>First leads to an increase in contraction </li></ul></ul><ul><ul><li>With time, leads to a decrease in contraction </li></ul></ul><ul><li>Increased heart rate leads to ischemia and decreased cardiac output </li></ul>Development of Congestive Heart Failure (cont’d)
  • 50. <ul><li>Beta-receptors in heart become less sensitive to sympathetic-nervous-system stimulation, decreasing heart rate and contractility </li></ul><ul><li>Alpha-receptors on peripheral blood vessels have increased sensitivity: </li></ul><ul><ul><li>Promoting vasoconstriction </li></ul></ul><ul><ul><li>Increasing cardiac workload </li></ul></ul>Development of Congestive Heart Failure (cont’d)
  • 51. <ul><li>Ventricular dilation leads to ventricular wall thinning, degeneration, and loss of contractility </li></ul>Development of Congestive Heart Failure (cont’d)
  • 52. <ul><li>Systolic dysfunction: </li></ul><ul><ul><li>Heart contracts with less force and can not pump out as much blood to the rest of the body as normal </li></ul></ul><ul><ul><li>Blood accumulates in the ventricles and veins </li></ul></ul>Types of Congestive Heart Failure
  • 53. <ul><li>Diastolic dysfunction: </li></ul><ul><ul><li>Heart is stiff and does not relax after contracting </li></ul></ul><ul><ul><li>Heart does not allow as much blood to enter its chambers from the veins, and the blood accumulates in the veins </li></ul></ul>Types of Congestive Heart Failure (cont’d)
  • 54. <ul><li>Left sided: </li></ul><ul><ul><li>More common </li></ul></ul><ul><ul><li>Fluid backs into lungs </li></ul></ul><ul><ul><li>Signs and symptoms include: </li></ul></ul>Types of Congestive Heart Failure (cont’d) <ul><li>Shortness of breath when lying down </li></ul><ul><li>Dyspnea </li></ul><ul><li> urine output </li></ul><ul><li>Syncope </li></ul><ul><li>Tachycardia </li></ul><ul><li>Dizziness </li></ul><ul><li>Pulmonary crackles </li></ul><ul><li>Activity intolerance </li></ul><ul><li>Coughing </li></ul><ul><li>Fatigue </li></ul>
  • 55. <ul><li>Right sided: </li></ul><ul><ul><li>Caused by pulmonary hypertension or right ventricular infarction </li></ul></ul><ul><ul><li>Fluid backs into rest of body, with abdominal organ congestion and peripheral edema </li></ul></ul><ul><ul><li>Signs and symptoms: </li></ul></ul>Types of Congestive Heart Failure (cont’d) <ul><li>Liver engorgement and right upper quadrant pain </li></ul><ul><li>Anorexia and nausea </li></ul><ul><li>Jugular venous distension </li></ul><ul><li>Lower extremity edema in the ambulatory </li></ul><ul><li>Sacral edema in the bedridden </li></ul>
  • 56. <ul><li>Biventricular (signs and symptoms of both left and right heart failure): </li></ul><ul><ul><li>Signs and symptoms: </li></ul></ul>Types of Congestive Heart Failure (cont’d) <ul><li>Nausea and vomiting </li></ul><ul><li> digestion and absorption of nutrients </li></ul><ul><li>Dysrhythmias </li></ul><ul><li>Cardiogenic shock or acute pulmonary edema </li></ul><ul><li>All symptoms of right and left heart failure </li></ul><ul><li>Dyspnea at rest </li></ul><ul><li>Hepatomegaly and splenomegaly </li></ul><ul><li> abdominal pressure </li></ul><ul><li>Ascites </li></ul><ul><li>Anorexia </li></ul>
  • 57. <ul><li>35%-55% of patients with moderately severe congestive heart failure (CHF) develop cardiac cachexia </li></ul><ul><li>Loss of lean body mass >10% of total weight </li></ul><ul><li>Resultant loss of cardiac muscle mass </li></ul><ul><li>Impaired fat absorption </li></ul>Cardiac Cachexia
  • 58. <ul><li>Many other metabolic changes: </li></ul><ul><ul><li>Decreased sodium </li></ul></ul><ul><ul><li>Increased catabolic catecholamines </li></ul></ul><ul><ul><li>Tumor necrosis factor—causes weight loss in animals and is increased in CHF patients </li></ul></ul>Cardiac Cachexia (cont’d)
  • 59. <ul><li>Diuretics </li></ul><ul><li>Dopamine </li></ul><ul><li>Analgesics </li></ul><ul><li>Antihypertensives </li></ul><ul><li>ACE inhibitors </li></ul><ul><li>Direct vasodilators </li></ul><ul><li>Antidysrhythmics </li></ul><ul><li>Cardiac glycosides (digitalis) </li></ul><ul><li>Aldosterone agonists </li></ul>Treatment of Coronary Heart Disease
  • 60. <ul><li>Antibiotics, if necessary </li></ul><ul><li>Iron supplementation, if necessary </li></ul><ul><li>Supplemental oxygen </li></ul><ul><li>Nitrates </li></ul><ul><li>Beta blockers </li></ul><ul><li>Anticoagulants </li></ul>Treatment of Coronary Heart Disease (cont’d)
  • 61. <ul><li>Arnold M. Heart failure. In: Merck Manual of Medical Information, Second Home Edition . Whitehouse Station, NJ: Merck Research Laboratories; 2003:150-158. </li></ul><ul><li>Hogan MA, Hill K. Pathophysiology: Reviews and Rationales . Upper Saddle River, NJ: Pearson Education; 2004:43-61. </li></ul><ul><li>Krummel DA. Medical nutrition therapy for heart failure and transplant. In: Mahan LK, Escott-Stump S. Krause’s Food, Nutrition, and Diet Therapy . 11th ed. Philadelphia, PA: WB Saunders; 2004:919-935. </li></ul><ul><li>Krummel DA. Medical nutrition therapy in cardiovascular disease. In: Mahan LK, Escott-Stump S. Krause’s Food, Nutrition, and Diet Therapy . 11th ed. Philadelphia, PA: WB Saunders; 2004:860-899. </li></ul><ul><li>Warnica JW. Coronary artery disease. In: Merck Manual of Medical Information, Second Home Edition . Whitehouse Station, NJ: Merck Research Laboratories; 2003:199-215. </li></ul>References and Recommended Readings

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